Pauling
and Rath contribute, with several published papers, to the understanding of the
molecular interactions resulting in the formation of atherosclerotic
plaques.Then they put the pieces
together to save the life of a critically ill colleague.This paper is a marvelous tour-de-force in
biochemical analysis. L-Lysine is the critical element. L-Proline is now
added to improve current (2011) arteriosclerosis treatments. The original Pauling paper is preserved by
John Ely of the University of Washington.It contains the essence of the solution to how to keep these plaques
from forming, to reverse their formation, and to produce an inexpensive dietary
cure for a large number of persons. Side note: Co-author, Matthias Rath,
(Germany) uses AA+L-Lysine+L-Proline+EGCG tocontrol
the spread of cancer.

This regimen was based on the hypothesis that, in
thrombotic atherosclerosis, lipoprotein(a) [Lp(a)]‹ size-heterogeneous, LDL-
like particles displaying independent risk activity for CAD ‹initiates plaque
formation by binding to fibrin in the damaged arterial wall. This postulated
mechanism correlates with the findings that apoliprotein(a) [apo(a)] has a
striking homology to plasminogen and the Lp(a) accumulates in atherosclerotic
lesions in the arteries of man (Rath et al., 1989)and the hypoascorbic guinea
pig (Rath and Pauling, 1990a, 1990b) and in occluded bypass venous grafts
(Cushing et al., 1989).

[I]t was known that Lp(a) binds to lysine-Sepharose,
immobilized fibrin and fibrinogen (Harpel et al., 1989); and the
epithelial-cell receptor for plasminogen ( Gonzalez-Gronow et al., 1989). This
binding specificity correlates with the genetic linkage on chromosome six and
striking homology of apo(a) and plasminogen ‹highly conserved multiple
kringle-four domains, a kringle-five domain, and a protease domain (McLean et
al., 1987).

Moreover, using the molecular evolutionary clock,
the loss in primates of the ability to synthesize ascorbate (Zuckerkandl and
Pauling, 1962; Rath and Pauling, 1990a) and acquisition of Lp(a) (Maeda et al.,
1983) both appear to have occurred about 40 million years ago.

These observations and the presence of Lp(a) in
sclerotic arteries (Rath et al., 1989; Rath and Pauling, 1990b) and in venous
grafts (Cushing et al., 1989) indicate that atherosclerosis may be initiated by
excess binding of Lp(a) to fibrin in vascular wall clots, thus interfering with
normal fibrinolysis by plasmin. This thrombogenic activity, which is postulated
to reside in plasmin-homologous domains of Lp(a), may help to stabilize the
damaged vascular wall, especially in ascorbate deficiency (Scanu, Lawn, and
Berg, 1991; Rath and Pauling, 1990a). Once bound to fibrin, the LDL-like domain
of Lp(a) could promote atheromas (Scanu, Lawn, and Berg, 1991).

In this scenario, high-dosage lysine could inhibit
or reverse plaque accretion by binding to Lp(a).

Independently, lysine benefits the heart as a
precursor with methionine in the synthesis of L-carnitine, the molecule that
carries fat into mitochondria for the synthesis of adenosine triphosphate (ATP)
bond energy needed for muscular and other cellular activities (Cederblad and
Linstedt, 1976). While his intake of 60 mg of CoQ-10, also required for ATP
synthesis, prior to the addition of lysine improved his sense of well being, it
did not suppress his angina.

Ascorbate without lysine also did not ameliorate
angina, but it is needed as an antioxidant to protect the vascular wall against
peroxidative damage and in hydroxylation reactions both in the synthesis of
carnitine and in the conversion of procollagen to collagen (hydroxylation of
prolyl and Iysyl residues) (Myllyla et al., 1984) to strengthen the
extracellular matrix of the wall.

Dosage:6 g
of ascorbate (acid form), 60 mg CoQ-10; a multivitamin tablet with minerals;
additional vitamins A, E and a B-complex; lecithin; and niacin, on advice of
his cardiologist to try to raise his HDL level.

Nevertheless, he still had to take nitroglycerin
sublingually to suppress angina during a daily two mile walk and when working
in his yard. This effort angina continued to worsen, imparting a feeling of
impending doom that was reinforced by his cardiologist's admonition during a check-up
in March 1991 that a fifth angiographic test and a fourth bypass operation were
no longer options. Also, the saphenous veins from his groin regions and legs
had all been used for previous grafts.

In this predicament and with his history of restenosis,
I suggested that he continue ascorbate and add 5 g of L-lysine daily (ca., six
times the lysine derived from dietary protein) to try to mitigate the
atherosclerotic activity of Lp(a). After reading the 1990 Rath and Pauling
reports and their manuscript titled "Solution to the puzzle of human
cardiovascular disease", he began taking 1 g of lysine in early May 1991
and reached 5 g (in divided doses eight hours apart) by mid-June. In mid-July,
his HDL was, as usual, a low 28 mg/dl. A low-normal 0.9 mg/dl blood creatinine
indicated that lysine could be increased, if needed.

He could now walk the same two miles and do yard
work without angina pain and wrote, "the effect of the lysine borders on
the miraculous". By late August, he cut up a tree with a chain saw, and in
early September started painting his house.

By late September, possibly from over-exertion, he
again began to have angina symptoms during his walks, but after stopping
strenuous work and increasing lysine to 6 g [calculated to provide a peak
280,000 molar excess in the blood over his then 6 mg/dl of Lp(a) to help
compensate for the relatively high dissociation constant of lysine-Lp(a)] these
symptoms stopped entirely by mid-October.

His blood creatinine was still a normal 1.2 mg/dl.
He attributes his newfound well being to the addition of lysine to his other
medications and vitamins. His wife and friends comment on his renewed vigor.

Whatever the patho-mechanisms of atherosclerosis,
the addition of lysine to medications and vitamins, including ascorbate,
markedly suppressed angina pectoris in this intractable case of CAD. [coronary
artery disease]